To mechanistically clarify how KRT19 regulates p21 protein stability in NSCLC cells, we focused on the potential proteins interacted with KRT19 in NSCLC cells using immunoprecipitation (IP) coupled with mass spectrometry (Fig. 6A-C), among which MYH9 showed high affinity enrichment and has been found to be dysregulated and oncogenic in many cancers [47–50]. This evidence concerns the gene CDKN1A and cancer.